Cardiac failure is a chronic clinical syndrome characterized by the heart being unable to adequately pump blood throughout the body. Generally, it is caused by any disease or condition that causes loss of cardiac tissue, especially of the left ventricle. The most common causes include cardiac infarction, coronary artery disease, myocarditis, chemotherapy, alcoholism and cardiomyopathy. On the other hand, cardiac failure may be caused by diseases or conditions that require an excessive demand for cardiac output. The most common causes include hypertension, valvular heart diseases (most often mitral insufficiency and aortic stenosis) and disorders of the thyroid gland. The long-term extra demand on the heart will lead to a compensatory hypertrophy of the cardiomyocytes. As the capillary network does not extend, hypertrophy will lead to a relative ischemia because the diffusion pathway for oxygen will increase. Recently, the importance of the role of ischemia in cardiac failure has been put forward (Van den Heuvel et al., 2000).
Thus far, the treatment of patients suffering from ischemic heart disease and subsequent cardiac damage leading to heart failure has focused on early reperfusion. Although additional cell protection therapy might, in theory, limit the damage that is caused by myocardial ischemia and hence, reduce morbidity and mortality, no sufficient therapies exist to date.
Additional supportive therapy to protect the myocardium in acute ischemic conditions consists nowadays in administration of beta-blockers, calcium antagonists and nitrates. However, these therapies have a low efficacy and alternative and/or additional strategies are needed.